Endothelial LRP1 regulates metabolic responses by acting as a co-activator of PPARγ

Hua Mao, Pamela Lockyer, Luge Li, Christie M. Ballantyne, Cam Patterson, Liang Xie and Xinchun Pi ()
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Hua Mao: Baylor College of Medicine
Pamela Lockyer: University of North Carolina at Chapel Hill
Luge Li: Baylor College of Medicine
Christie M. Ballantyne: Center for Cardiovascular Disease Prevention, Methodist DeBakey Heart and Vascular Center, Section of Cardiovascular Research, Baylor College of Medicine
Cam Patterson: New York-Presbyterian Hospital
Liang Xie: Baylor College of Medicine
Xinchun Pi: Baylor College of Medicine

Nature Communications, 2017, vol. 8, issue 1, 1-11

Abstract: Abstract Low-density lipoprotein receptor-related protein 1 (LRP1) regulates lipid and glucose metabolism in liver and adipose tissue. It is also involved in central nervous system regulation of food intake and leptin signalling. Here we demonstrate that endothelial Lrp1 regulates systemic energy homeostasis. Mice with endothelial-specific Lrp1 deletion display improved glucose sensitivity and lipid profiles combined with increased oxygen consumption during high-fat-diet-induced obesity. We show that the intracellular domain of Lrp1 interacts with the nuclear receptor Pparγ, a central regulator of lipid and glucose metabolism, acting as its transcriptional co-activator in endothelial cells. Therefore, Lrp1 not only acts as an endocytic receptor but also directly participates in gene transcription. Our findings indicate an underappreciated functional role of endothelium in maintaining systemic energy homeostasis.

Date: 2017
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DOI: 10.1038/ncomms14960

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